Centrosome duplication is a critical step in assembly of the bipolar mitotic spindle, but the molecular mechanisms regulating this process during the cell cycle and during animal development are poorly understood. Here, we report that the zyg-1 gene of Caenorhabditis elegans is an essential regulator of centrosome duplication. ZYG-1 is a protein kinase specifically required for daughter centriole formation that localizes transiently to centrosomes and acts at least one cell cycle prior to each spindle assembly event. In the embryo, ZYG-1 participates in a unique regulatory scheme whereby paternal ZYG-1 regulates duplication and bipolar spindle assembly during the first cell cycle, and maternal ZYG-1 regulates these processes thereafter. ZYG-1 is therefore a key molecular component of the centrosome/centriole duplication process.
Centrosomes are major determinants of mitotic spindle structure, but the mechanisms regulating their behavior remain poorly understood. The spd-2 gene of C. elegans is required for centrosome assembly or "maturation." Here we show that spd-2 encodes a coiled-coil protein that localizes within pericentriolar material (PCM) and in the immediate vicinity of centrioles. During maturation, SPD-2 gradually accumulates at the centrosome in a manner that is partially dependent on Aurora-A kinase and cytoplasmic dynein. Interestingly, SPD-2 interacts genetically with dynein heavy chain and SPD-5, another coiled-coil protein required for centrosome maturation. SPD-2 and SPD-5 are codependent for localization to the PCM, but SPD-2 localizes to centrioles independently of SPD-5. Surprisingly, we also find that SPD-2 is required for centrosome duplication and genetically interacts with ZYG-1, a kinase required for duplication. Thus, we have identified SPD-2 as a factor critical for the two basic functions of the centrosome-microtubule organization and duplication.
Caenorhabditis elegans has two genes, unc-59 and unc-61, encoding septin-family GTPases. Mutations in the septin genes cause defects in locomotory behavior that have been previously attributed to cytokinesis failures in postembryonic neuroblasts. We find that mutations in either septin gene frequently cause uncoordination in newly hatched larvae in the absence of cytokinesis failures. The septins exhibit developmentally regulated expression, including expression in various neurons at times when processes are extending and synapses are forming. Motor neurons in the mutant larvae display defects in multiple aspects of axonal migration and guidance that are likely to be responsible for the locomotory behavior defects. The septins are also expressed in migrating distal tip cells, which are leaders for gonad arm extension. Septin mutants affect morphology of the distal tip cells, as well as their migration and guidance during gonadogenesis. These results suggest that septins may be generally required for developmental migrations and pathfinding.
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